ライフサイエンスコーパス: IPSC

1 IPSC bursts were identical in the absence of TTX, althou

2 IPSC latency and rise time were also strongly dependent

3 IPSC responses to trains of stimuli were recorded in con

4 IPSCs and EPSCs show rapid acceleration during developme

5 IPSCs arriving in pairs of either pyramidal or fast-spik

6 IPSCs evoked from the NAc were potently inhibited by act

7 -2 stimulation within the RMTg evoked GABA-A IPSCs in dopamine neurons that were inhibited by mu-opio

8 se in the brain through inhibition of GABA-A IPSCs onto dopamine cells.

9 Additional recordings of GABA-A IPSCs showed CRF-R2 activation-facilitated presynaptic r

10 revealed that the laserspritzer-induced AAS-IPSCs persisted in the presence of TTX and TEA but not 4

11 hibitory postsynaptic currents (IPSCs) along IPSC trains evoked by the 5 Hz electrical stimulation, b

12 tors, which prolonged the duration of alpha2-IPSCs when multiple release sites were activated synchro

13 relationship between subunit composition and IPSC decay is less clear.

14 al analysis of changes in miniature EPSC and IPSC properties in L2 pyramidal neurons showed that mEPS

15 Both EPSCs and IPSCs have slow kinetics in prehearing animals, which du

16 matures by postnatal day 20, with EPSCs and IPSCs having fast kinetics.

17 stimulation in either ear produced EPSCs and IPSCs in most neurons.

18 We recorded EPSCs and IPSCs to examine the buildup of neuronal activity preced

19 Ganglion cell EPSCs and IPSCs were monitored to measure the output of bipolar an

20 EPSCs and IPSCs were well correlated except in center-preferred ne

21 ic currents (combined simultaneous EPSCs and IPSCs) became markedly depolarized during the preictal p

22 sity and in evoked and spontaneous EPSCs and IPSCs.

23 PSCs evoked from the RMTg, 18% from NAc, and IPSCs evoked from VTA interneurons were almost insensiti

24 aptic current (IPSC) in a PN and an autaptic IPSC.

25 omputational analysis indicated that GABA(B) IPSCs can phasically modulate the discharge of PT intern

26 y modulate amplitude and duration of GABA(B) IPSCs.

27 CB(1) receptor antagonists enhanced basal IPSCs in CA1 pyramidal neurons in MAGL(-)/(-) mice, whil

28 group II/III mGluR activation decreases both IPSC frequency and I(GABA)tonic amplitude.

29 concentration-dependent enhancement of both IPSC frequency and tonic GABA(A) current (I(GABA)tonic)

30 butes contrast with large cells, whose brief IPSCs and rapid firing rates can permit well timed posti

31 se, interneuronal excitability was high, but IPSCs, evoked by local stimulation, or osmotically by hy

32 In mutant CbN cells, IPSC kinetics were unchanged, but mutant males, unlike f

33 neurons, strong focal shocks evoked compound IPSCs indicating convergent summation of multiple inhibi

34 In contrast, IPSC amplitude did not differ between cell types.

35 ed than excitatory ones, but that correlated IPSCs arise from the activation of common presynaptic in

36 This inhibitory postsynaptic current (IPSC) erosion resulted from a failure of the astrocytic

37 diated slow inhibitory postsynaptic current (IPSC) in a PN and an autaptic IPSC.

38 or-mediated inhibitory postsynaptic current (IPSC) that resulted in only a transient pause in firing.

39 al cells, we found that inhibitory currents (IPSCs) are more correlated than excitatory ones, but tha

40 ression of inhibitory postsynaptic currents (IPSCs) along IPSC trains evoked by the 5 Hz electrical s

41 ecrease in inhibitory postsynaptic currents (IPSCs) and an increase in the AMPAR/NMDAR ratio in ventr

42 e decay of inhibitory postsynaptic currents (IPSCs) and induce spontaneous GlyR activation.

43 ression of inhibitory postsynaptic currents (IPSCs) followed by modest long-term depression (I-LTD) i

44 2-receptor inhibitory postsynaptic currents (IPSCs) in GIRK2-expressing MSNs that occurred in under a

45 tiation of inhibitory postsynaptic currents (IPSCs) in hypoglossal motoneurons and its modulation by

46 -frequency inhibitory postsynaptic currents (IPSCs) in pyramidal cells, even with glutamatergic trans

47 B-mediated inhibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were m

48 ression of inhibitory postsynaptic currents (IPSCs) induced by D(2) dopamine receptor and cannabinoid

49 of evoked inhibitory postsynaptic currents (IPSCs) mediated by D1-type receptors seen in wild-type m

50 miniature inhibitory postsynaptic currents (IPSCs) of lamina II neurons.

51 GABAergic inhibitory postsynaptic currents (IPSCs) recorded from neurons in the mouse ventral tegmen

52 ontaneous inhibitory post-synaptic currents (IPSCs) in MSNs.

53 nsmission (inhibitory postsynaptic currents, IPSCs) in the DR.

54 he guinea pig determined the duration the D2-IPSC.

55 Evoked D2-IPSCs could be driven by repetitive stimulation and were

56 Functionally, differences in D2-IPSCs resulted in inhibition of dopamine neuron firing o

57 dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mouse, rat, and guinea pig.

58 ime course of D2-receptor-mediated IPSCs (D2-IPSCs) was consistent between cells and was unaffected b

59 with cocaine extended the time course of D2-IPSCs and suggested that transporters strongly limited s

60 This resulted in an increased duration of D2-IPSCs in the guinea pig.

61 tributed independently to the duration of D2-IPSCs.

62 Robust D2-IPSCs were observed in all recordings from neurons in sl

63 urons in slices taken from mouse, whereas D2-IPSCs in rat and guinea pig were observed less frequentl

64 ors, was responsible for the slowly decaying IPSCs.

65 prisingly, decreased depression of dendritic IPSCs isolated after blocking GABAa receptor on the soma

66 alter the kinetics of the dopamine-dependent IPSC.

67 vivo induction of AT at around P20 disrupted IPSC and EPSC integration in the LSO, so that 1 week lat

68 in perisomatic synapses, suggesting distinct IPSC decay kinetics.

69 Cholinergically driven IPSCs were not affected by ablation of striatal fast-spi

70 ency of spontaneous, action potential-driven IPSCs.

71 exogenous glutamine administration enhanced IPSCs.

72 ine neurons from adult rats exhibit enhanced IPSCs after adolescent alcohol exposure corresponding to

73 ic IPSCs facilitate to maintain a fixed EPSC-IPSC ratio during short-term plasticity.

74 ors by iontophoresis of ATP decreased evoked IPSC amplitudes and action potential-evoked calcium tran

75 Evoked IPSCs (eIPSCs) mediated by GABAA receptors were isolated

76 2 agonist but not D1 agonist, on both evoked IPSCs and EPSCs, were reduced.

77 uency spiking in single granule cells evoked IPSCs in approximately 5% of neighboring granule cells,

78 ative perisomatic, but not dendritic, evoked IPSCs were significantly reduced in these mice.

79 ta3-KO mice exhibited attenuated GABA-evoked IPSCs.

80 While CCh has been shown to inhibit evoked IPSCs in other systems, this effect is intriguing in tha

81 In this preparation, light-evoked IPSCs could only reach axotomized BC terminals via the l

82 d a unique preparation to study light-evoked IPSCs recorded from axotomized terminals of ON-type mixe

83 ta, agonists reduced the amplitude of evoked IPSCs and appeared to colocalize in a significant portio

84 proximately 70%; (2) the amplitude of evoked IPSCs and isoguvacine-evoked current increased by approx

85 sized that CCh-mediated inhibition of evoked IPSCs might be produced by activity-dependent increases

86 n this system; however, inhibition of evoked IPSCs produced by both 3 and 10 mum CCh is insensitive t

87 NO-711 (1 mum) produces inhibition of evoked IPSCs that is reversed by CGP52432, and that lower doses

88 of a low baseline quantal content of evoked IPSCs using whole cell patch-clamp recordings from hypog

89 c mice the dopaminergic modulation of evoked IPSCs was shifted, with reduced sensitivity.

90 Cs, whereas the paired-pulse ratio of evoked IPSCs was unaffected, suggesting that the absence of Cx3

91 ell axon collaterals had no effect on evoked IPSCs measured in synaptically coupled Purkinje cells.

92 ion of AgRP neurons reliably produced evoked IPSCs in POMC neurons, leading to the inhibition of POMC

93 ytosis is not apparent when recording evoked IPSCs in the presence of AM251, suggesting that the exoc

94 ctivation of receptors contributed to evoked IPSCs, serotonin reuptake transporters prevented pooling

95 ne in GlyT2-Cre transgenic mice, evoked fast IPSCs in principal cells.

96 ming on the scale of milliseconds, only fast IPSCs can enhance the detection of narrowband acoustic s

97 ON and OFF L-IPSCs, like reciprocal feedback IPSCs, were mediated by both GABA(A) and GABA(C) recepto

98 Consistent with these findings, IPSCs recorded from high-frequency OHCs that express BK

99 ing a switch from Glyalpha2 to Glyalpha1 for IPSCs and increased expression of GluA3 and GluA4 subuni

100 The low-frequency IPSC oscillations induced by CCh or optogenetically stim

101 wever, this had no effect on theta-frequency IPSC rhythms induced by carbachol (CCh).

102 had no effect on evoked or spontaneous GABA IPSCs.

103 D1)-mediated long-term potentiation of GABAA-IPSCs (D1-LTPGABA) in the oval bed nucleus of the stria

104 ted inhibitory postsynaptic currents (GABAAR IPSCs) is associated with reduced EtOH consumption.

105 st robust DPDPE-induced inhibition of GABAAR IPSCs in VTA neurons.

106 ulation of drinking and inhibition of GABAAR IPSCs, we examined whether these changes can be predicte

107 In these motoneurons, EPSCs and GABAergic IPSCs were blocked by the application of CNQX, AP-5 and

108 (p = 0.003, n = 26) and augmented GABAergic IPSCs in CVNs by 21 +/- 5% (p = 0.001, n = 26).

109 on of VP neuron terminals elicited GABAergic IPSCs in both dopamine (DA) and non-DA VTA neurons, and

110 TRN neurons and their axons evokes GABAergic IPSCs in TRN neurons in mice younger than 2 weeks of age

111 UBC relay, whereas large and fast GABAergic IPSCs may in addition control spike timing in mGluRII-ne

112 und that the emerged DOR inhibited GABAergic IPSCs through both the phospholipase A(2) (PLA(2)) and c

113 rginine nor SNAP had any effect on GABAergic IPSCs.

114 st-spiking interneurons, recurrent GABAergic IPSCs predominated interictally and during the early pre

115 eased the frequency of spontaneous GABAergic IPSCs without changes in their amplitudes.

116 Surprisingly, unitary GABAergic IPSCs were only weakly calcium dependent.

117 increase in glycinergic, but not GABAergic, IPSCs in CVNs.

118 isetron, significantly increases glycinergic IPSC decay times without causing motor side effects.

119 Glycinergic IPSCs were evoked by threshold stimulation of inhibitory

120 eptor (NMDAR)-mediated EPSCs and glycinergic IPSCs.

121 reased the frequency of isolated glycinergic IPSCs by 27 +/- 8% (p = 0.003, n = 26) and augmented GAB

122 shed the effect of L-arginine on glycinergic IPSCs but not on evoked monosynaptic EPSCs.

123 We propose that slow glycinergic IPSCs may provide an inhibitory tone, setting the gain o

124 We show that glycinergic IPSCs are present in all cells.

125 In contrast, GlyR IPSC and NMDAR-EPSC decay times were unchanged.

126 pting pyramidal neurons, and also had higher IPSC and EPSC frequencies than adapting neurons.

127 However, IPSC decays evoked by axo-axonic, parvalbumin- or cholec

128 local release of serotonin generated 5-HT1A -IPSCs in serotonin neurons that rose and fell within a s

129 As a result, the decay of 5-HT1A -IPSCs was independent of the intensity of stimulation or

130 The duration of 5-HT1A -IPSCs was primarily shaped by receptor deactivation due

131 ed inhibitory postsynaptic currents (5-HT1A -IPSCs) generated by the activation of G-protein-coupled

132 extrasynaptic space from activating 5-HT1A -IPSCs.

133 holinergic-evoked inhibition, and a delay in IPSC latency.

134 We also rule out small increases in IPSC decay times (as caused by W170S and R414H) as a pos

135 by the inefficiency of carbachol to increase IPSC frequency in these cells.

136 notropic GluRs and nAChRs blocked, increased IPSCs in MTCs and ETCs, indicating that mAChRs recruit g

137 of adenosine receptors selectively increased IPSCs evoked from the NAc during morphine withdrawal.

138 Rs in the presence of tetrodotoxin increased IPSCs in all glomerular neurons, indicating action poten

139 The Abeta-induced IPSC decline could be prevented with intracellular appli

140 activation accounted for 15% of interneuron IPSC amplitude, while the remaining current was mediated

141 at the interneurons elicited GABAergic IPSPs/IPSCs in spiny neurons powerful enough to significantly

142 This biphasic form of L-IPSC plasticity may underlie adaptation and sensitizatio

143 rvals (PPIs) of 50 and 300 ms, whereas OFF L-IPSC latencies decreased at the 300 ms PPI.

144 hat light evokes ON and OFF lateral IPSCs (L-IPSCs) in Mb terminals having different temporal pattern

145 erm plasticity of GABAergic lateral IPSCs (L-IPSCs).

146 stic changes in the strength and timing of L-IPSCs help to dynamically shape the time course of gluta

147 Short-term plasticity of L-IPSCs may thus influence the strength, timing, and spati

148 Bright light stimulation evoked ON and OFF L-IPSCs in axotomized BCs, which had distinct onset latenc

149 depression at intervals <1 s, whereas OFF L-IPSCs showed depression at intervals </=1 s and amplitud

150 ibution of rods versus cones to ON and OFF L-IPSCs was light intensity dependent.

151 AMPARs differentially affected ON and OFF L-IPSCs, confirming that these two types of feedback inhib

152 ON and OFF L-IPSCs, like reciprocal feedback IPSCs, were mediated by

153 paired light stimulation, latencies of ON L-IPSCs increased at paired-pulse intervals (PPIs) of 50 a

154 ON L-IPSCs showed paired-pulse depression at intervals <1 s,

155 h the synaptic strength and latency of the L-IPSCs.

156 e short-term plasticity of GABAergic lateral IPSCs (L-IPSCs).

157 e found that light evokes ON and OFF lateral IPSCs (L-IPSCs) in Mb terminals having different tempora

158 ing alpha-subunit of BK channels have longer IPSCs than do the OHCs of BKalpha(+/+) littermates.

159 mputational modelling confirmed that matched IPSC and EPSC kinetics are required to generate mature i

160 ong-lasting enhancement of feedback-mediated IPSC/Ps in the projection neurons, which persists for th

161 sponse was a slow, GABA(A) receptor-mediated IPSC that has not been previously described in striatum

162 resulting dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mouse, rat, and guinea pi

163 Enhanced GABA(B)-mediated IPSCs are critical for the generation of generalized tha

164 Here, we demonstrate that GABA(B)-mediated IPSCs recorded in the thalamus are primarily defined by

165 mate-mediated EPSCs as well as GABA-mediated IPSCs, although the net effect of neurotransmitter relea

166 dependent currents, slower Purkinje-mediated IPSCs, and lower spontaneous firing rates, but rotarod p

167 rea, the time course of D2-receptor-mediated IPSCs (D2-IPSCs) was consistent between cells and was un

168 ged the duration of alpha2-receptor-mediated IPSCs even when reuptake was intact.

169 GABA(A) receptor-mediated IPSCs evoked by electrical or optogenetic stimulation of

170 , and monosynaptic GABA(A) receptor-mediated IPSCs were elicited.

171 led a reduction in spontaneous and miniature IPSC frequency after head injury; no concurrent change i

172 hibitory short-term plasticity and miniature IPSC frequency and amplitude were normal in Cntnap2(-/-)

173 rong positive relationship between miniature IPSC frequency and the occurrence of both stereotyped ex

174 Miniature IPSCs in Cre(+) PCs were insensitive to low concentratio

175 evious reports of larger amplitude miniature IPSCs and larger BC-->GC quantal size.

176 d in pilocarpine-treated mice, and miniature IPSCs were reduced, paralleling the decrease in CCK-labe

177 n the frequency of spontaneous and miniature IPSCs, an effect completely abolished by the GABAA recep

178 Moreover, FS-->SP evoked miniature IPSCs increased in deprived hemispheres when MD was init

179 naptic signaling, we recorded GABA miniature IPSCs (mIPSCs) from cultured rat cerebellar granule cell

180 adjuvant (CFA) increased GABAergic miniature IPSCs (mIPSCs).

181 nsities of spontaneous glycinergic miniature IPSCs (mIPSCs) were significantly smaller in the G93A-SO

182 miniature EPSCs with no change in miniature IPSCs, indicating that overexpression of MeCP2 selective

183 miniature EPSCs and interestingly, miniature IPSCs.

184 changes in inhibition by measuring miniature IPSCs (mIPSCs) in layer 2/3 pyramidal neurons of mouse v

185 verage amplitude of GABAA-mediated miniature IPSCs (mIPSCs) in these neurons is enhanced for several

186 less frequent spontaneous but not miniature IPSCs.

187 combining whole-cell recordings of miniature IPSCs (mIPSCs) and quantitative immunolocalization of sy

188 er Cd(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by approximately 50%, su

189 Specifically, the amplitude of miniature IPSCs (mIPSCs) was decreased after 21 d withdrawal from

190 that IPSC bursts were composed of miniature IPSCs (mIPSCs), and that the probability of burst genera

191 icantly increased the frequency of miniature IPSCs (mIPSCs).

192 andamide increase the frequency of miniature IPSCs (mIPSCs)recorded from hilar mossy cells without al

193 ecordings revealed the presence of miniature IPSCs in Cre(+) layer 2/3 pyramidal cells (PCs) with unc

194 ted the amplitude distributions of miniature IPSCs, whereas the paired-pulse ratio of evoked IPSCs wa

195 ects of ex vivo ethanol (50 mM) on miniature IPSCs (mIPSCs) in the DR 24-h post-ethanol exposure.

196 ing amplitude and had no effect on miniature IPSCs or EPSCs.

197 equency of tetrodotoxin-resistant, miniature IPSCs (mIPSCs) in 67% of DMV neurons recorded in acutely

198 in-, and 4-aminopyridine-sensitive miniature IPSCs (mIPSCs) mediated by GABA(A) receptors.

199 ons without changes in spontaneous miniature IPSCs (mIPSCs).

200 but less well than the summation of monaural IPSCs.

201 minimal focal shocks activated monosynaptic IPSCs at fixed latency (low jitter) that often failed (3

202 , LSP4-2022 also reduced evoked monosynaptic IPSCs in CA1 pyramidal cells and, in contrast to its eff

203 ergic LH --> PVH fibers induced monosynaptic IPSCs in PVH neurons, and potently increased feeding, wh

204 sted DMV preganglionic neurons (PGNs) but no IPSCs.

205 -Astrocyte autaptic evoked EPSCs, but not IPSCs, displayed an altered temporal profile, which incl

206 . WT neurons and a DPDPE-induced decrease of IPSC frequency revealed a role for DOPs.

207 In the dLGN, enhancement of IPSC frequency and I(GABA)tonic by group I mGluRs is not

208 Inhibition of IPSC frequency by morphine was also reduced in beta-arr2

209 In 25% of dual recordings, a subset of IPSC bursts were highly synchronized in onset in pairs o

210 However, we recorded endogenous bursts of IPSCs in hypothalamic magnocellular neurones in the pres

211 5 subtypes, the mGluR-dependent component of IPSCs elicited by intrastriatal electrical stimulation i

212 s demonstrate that diversity in the decay of IPSCs can be generated by varying the expression of diff

213 Cs and a 5.3-fold difference in the decay of IPSCs elicited by single-pulse stimulus.

214 llular Ca2+ with Sr2+ increased the decay of IPSCs in LF neurons, and EGTA-AM reduced the decay of IP

215 LF neurons, and EGTA-AM reduced the decay of IPSCs in MF/HF neurons.

216 rons (PV-IPSCs), but decreased depression of IPSCs from dendritically projecting somatostatin cells (

217 ic analyses revealed increased depression of IPSCs originating from perisomatically projecting parval

218 CB(1) receptor agonist-induced depression of IPSCs was decreased in MAGL(-)/(-) mice.

219 arly component of DHPG-induced depression of IPSCs was mediated by the cannabinoid CB1 receptors, whi

220 The facilitation of IPSCs produced by direct cAMP stimulation was unaffected

221 lient observation was a reduced frequency of IPSCs and EPSCs, whereas the amplitudes were not modifie

222 These data suggest that inhibition of IPSCs by morphine involves a beta-arr2/c-Src mediated me

223 Morphine induced a 46% inhibition of IPSCs evoked from the RMTg, 18% from NAc, and IPSCs evok

224 d, moreover, show that the decay kinetics of IPSCs are slowed in mature animals.

225 The kinetics of IPSCs influence many neuronal processes, such as the fre

226 p recordings, the amplitudes and kinetics of IPSCs mediated by AASs were similar to those mediated by

227 By examining the decay kinetics of IPSCs, we found that while spillover may allow for the a

228 Furthermore, the reversal potential of IPSCs, which was not significantly altered during withdr

229 o determine if the frequency potentiation of IPSCs occurs as a consequence of a low baseline quantal

230 Our data demonstrate the presence of IPSCs and the synaptic enrichment of the alpha1 and beta

231 ptors matches the pharmacological profile of IPSCs.

232 The simultaneous reduction of IPSCs and increase in membrane resting potential produce

233 jected into an ET cell evoked suppression of IPSCs.

234 ation frequency was only weakly dependent on IPSC amplitude, and decreased to that of CA3 slow gamma

235 enhanced the DOP receptor-induced effect on IPSCs via presynaptic mechanisms.

236 However, there was little or no effect on IPSCs.

237 near synapses and selectively modulate peak IPSC amplitude, which is primarily dependent on perisyna

238 principal cells paced by recurrent perisomal IPSCs.

239 nergic nerve endings to mediate fast, phasic IPSCs.

240 ion in the frequency and amplitude of phasic IPSCs, tonic inhibitory currents, as well as in the numb

241 oth facilitating and depressing polysynaptic IPSCs, indicating that this robust inhibition is not cau

242 the juvenile CA3 that MF-driven polysynaptic IPSCs facilitate to maintain a fixed EPSC-IPSC ratio dur

243 -R2 agonists to depress EPSCs and potentiate IPSCs was diminished.

244 l effects of dyes were sufficient to prolong IPSCs and to dampen network activity in multielectrode a

245 Zolpidem prolongs IPSCs to decrease sleep latency and increase sleep time,

246 ally projecting parvalbumin interneurons (PV-IPSCs), but decreased depression of IPSCs from dendritic

247 sed the sensitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist baclofen.

248 quency stimulation of SC afferents to reduce IPSC amplitudes.

249 reased to that of CA3 slow gamma by reducing IPSC decay rate or reducing interneuron activation throu

250 also known as Kir3) channels mediate a slow IPSC and control the excitability of DA neurons.

251 Although fast and slow IPSCs in T-stellate cells improve spike timing on the sc

252 mulation evokes large GABA(B)R-mediated slow IPSCs in perisomatic-targeting (PT) PVIs, but only small

253 pus, where they prolong the duration of slow IPSCs in pyramidal cells.

254 tero-oligomers increase the duration of slow IPSCs.

255 Computer models reveal that slow IPSCs in bushy cells can improve spike timing on the sca

256 -CF (MF/HF) neurons had significantly slower IPSCs, with a 2.6-fold difference in the decay time cons

257 ritically projecting somatostatin cells (SOM-IPSCs).

258 anwhile, OF decreased the sensitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist bacl

259 Our results suggest that target-specific IPSC kinetics are critical for the segregated parallel p

260 tion to prolonging miniature and spontaneous IPSC interevent intervals, brain injury significantly re

261 i), our results showed increased spontaneous IPSC frequency and amplitude in MSNs as well as in the m

262 TRH increased spontaneous IPSC frequency without affecting amplitude and had no ef

263 Morphine inhibited spontaneous IPSC frequency, mainly through MOPs, with only a negligi

264 vealed rhythmic, large amplitude spontaneous IPSCs that had a similar frequency, pattern and opioid s

265 and alters cell capacitance and spontaneous IPSCs amplitude of AVPV/PeN and Arc Kiss1 populations in

266 Antagonism of ASIC1a decreased spontaneous IPSCs more than EPSCs, and increased the excitability of

267 principal neurons, and increased spontaneous IPSCs recorded from principal cells significantly more t

268 GABA-mediated spontaneous IPSCs (sIPSCs) in POMC neurons were unaffected by distur

269 carbachol-induced enhancement of spontaneous IPSCs (sIPSCs) originating from CCK-containing basket ce

270 ust decrease in the frequency of spontaneous IPSCs (sIPSCs).

271 nd reduction in the amplitude of spontaneous IPSCs (sIPSCs).

272 e in the decay time constants of spontaneous IPSCs and a 5.3-fold difference in the decay of IPSCs el

273 pirole, whereas the amplitude of spontaneous IPSCs was increased by quinpirole but not dopamine.

274 uced at P12-13, whereas those of spontaneous IPSCs were significantly increased at P12-13; and (5) bo

275 ptors inhibited the frequency of spontaneous IPSCs.

276 a-ARs increased the frequency of spontaneous IPSCs; however, this effect was smaller and confined to

277 ABA transporter has no effect on spontaneous IPSCs recorded in TRN neurons aged 2 weeks or older whil

278 lation at 20-150 Hz evoked greatly summating IPSCs.

279 depolarizing steps significantly suppressed IPSCs induced by application of the cholinergic agonist

280 Cs that express BK channels are briefer than IPSCs recorded from low-frequency (apical) OHCs that do

281 incidence increased 5-fold, indicating that IPSC bursts were composed of miniature IPSCs (mIPSCs), a

282 The IPSC difference between pyramidal subtypes was activity

283 In contrast, the IPSC decay time constant depended only on the postsynapt

284 The IPSCs are regulated by exogenous and endogenous cannabin

285 onged the rise and reduced the amplitude the IPSCs and the effects were potentiated when uptake was i

286 Bath-applied Abeta (1 mum) depressed the IPSCs on average to 60% of control, whereas a reversed s

287 tro, it evoked a transient depression of the IPSCs.

288 lover plays a greater role in prolonging the IPSCs of MF/HF neurons.

289 d a synergistic DOR-MOR interaction in their IPSC inhibition, which was dependent on upregulated acti

290 These IPSCs then decreased to zero or reversed polarity by the

291 amine (DA) and non-DA VTA neurons, and these IPSCs were inhibited by the mu opioid receptor agonist D

292 The slow kinetics of these IPSCs was likely caused by the low concentration and spi

293 we show that the waveform of randomly timed IPSCs (evoked by high extracellular potassium) in high-f

294 ation profile of agonists underlying the two IPSCs.

295 o measured kinetic properties of the unitary IPSC: latency, rise time, and decay time constant.

296 Furthermore, unitary IPSCs recorded at IS3-OLM synapses had a small amplitude

297 1 at GABAergic synapses, we recorded unitary IPSCs (uIPSCs) at cholecystokinin-expressing interneuron

298 ch differences were especially dramatic when IPSCs were elicited by train stimulations at physiologic

299 mate release only in TRPV1+ neurons, whereas IPSC rates were unaffected.

300 of presynaptic adenosine receptors, whereas IPSCs evoked from RMTg were not changed.